Body mass has a paradoxical effect on mortality in RA. Patients with high BMI have lower mortality than thinner patients. This effect is mediated in part by comorbidity. The effect of body mass on survival seems to be modified by the level of systemic inflammation.

Objective. To estimate the contribution of cardiovascular (CV) risk factors and rheumatoid arthritis (RA) disease manifestations to atherosclerosis in RA.Methods. We used high-resolution carotid ultrasound to measure the carotid intima-media thickness (IMT) and plaque in 631 RA patients. Using R 2 measures from multivariable models, we estimated the contribution of demographic characteristics (age, sex, and ethnic group), CV risk factors (diabetes mellitus, hypercholesterolemia, cigarette smoking, hypertension, and body mass index, and RA manifestations (joint tenderness, swelling, and deformity, nodules, erythrocyte sedimentation rate [ESR], C-reactive protein, rheumatoid factor, the HLA-DRB1 shared epitope, and cumulative glucocorticoid dose) to each of the outcomes. Estimates were obtained in the full sample, and within strata defined by age, sex, and ethnic group. We tested for interaction between CV risk factors and RA manifestations.Results. The contribution of demographic factors, CV risk factors, and RA manifestations to IMT and plaque R 2 varied depending on the patients' age stratum. Demographic features explained 11-16% of IMT variance, CV risk factors explained 4%-12%, and RA manifestations explained 1-6%. The greatest contribution of RA manifestations occurred in the youngest age group, while that of CV risk factors occurred in the older age groups. Results for carotid plaque were similar. There was a significant interaction between the number of CV risk factors present and the ESR, suggesting that the ESR's effect on IMT varied according to the number of CV risk factors.Conclusion. Both established CV risk factors and manifestations of RA inflammation contribute significantly to carotid atherosclerosis in RA, and may modify one another's effects. These findings may have implications regarding the prevention of atherosclerosis in RA.The mechanism underlying the high frequency of cardiovascular (CV) morbidity that occurs in rheumatoid arthritis (RA) is not completely understood (1-16). Earlier studies have indicated that the excess CV event rate in RA is not explained by an excess of established CV risk factors (17,18). Those studies did not address whether these risk factors operate similarly in RA as they do in the general population.Diabetes mellitus, hypercholesterolemia, hypertension, cigarette smoking, and obesity are powerful classifiers of CV risk (19). One or more established CV risk factors are present in at least 80% of people with symptomatic coronary artery disease in the general population (20). The prevalence is even higher, approaching 100%, among persons with fatal myocardial infarction (21).People with and those without RA have similar CV risk factor profiles (17,18,22). The resemblance suggests that established CV risk factors may play an important role in the CV morbidity that occurs in RA, as they do in the general population. In earlier studies that

Objective. Glucocorticoids are suspected to cause atherosclerosis. Because of the possibility that their antiinflammatory effect may be antiatherogenic, this study investigated the effect of glucocorticoids on the arteries of patients with rheumatoid arthritis (RA).Methods. We assessed the arteries of 647 patients with RA. Central atherosclerosis was measured using high-resolution carotid ultrasound for the presence of plaque and for the extent of carotid artery intima-media thickness (CaIMT). Peripheral atherosclerosis was assessed using the systolic pressures of the dorsal pedal, posterior tibial, and brachial arteries to obtain the ankle-brachial index (ABI). Cumulative glucocorticoid dose was determined using pharmacy records, supplemented by self-report. Cardiovascular (CV) risk factors and RA clinical manifestations were ascertained using clinical and laboratory methods.Results. Among the RA patients studied, 427 (66%) had received glucocorticoids. Of those who had never received glucocorticoids, 100 (47%) of 215 had carotid plaque and 17 (8%) of 219 had >1 incompressible lower-limb artery (ABI >1.3). Among patients in the highest tertile of lifetime glucocorticoid exposure (>16.24 gm prednisone), the frequency of carotid plaque increased to 85 (62%) of 138 (P ‫؍‬ 0.006) and that of lower-limb arterial incompressibility increased to 24 (17%) of 140 (P ‫؍‬ 0.008), with differences remaining significant after adjustment for age at onset, disease duration, sex, CV risk factors, and RA clinical manifestations (tender, swollen, and deformed joint counts, subcutaneous nodules, rheumatoid factor seropositivity, and erythrocyte sedimentation rate). The CaIMT also displayed an increase with higher glucocorticoid exposure, but the differences did not reach significance. Lower-limb artery obstruction (ABI <0.9) was not associated with glucocorticoid exposure.Conclusion. In this RA sample, glucocorticoid exposure was associated with carotid plaque and arterial incompressibility, independent of CV risk factors and RA clinical manifestations. This supports a role for glucocorticoids in the CV complications that occur in RA.

Anti-CCP antibodies and the RF may be pathogenically related to ILD. The association between ILD and smoking is dependent on the HLA-DRB1 SE, which may reflect gene-environment interaction.

Background: Despite increased cardiovascular morbidity and mortality in rheumatoid arthritis, the peripheral arteries remain understudied. Objective: To examine the lower limb arteries in age and sex matched, non-smoking subjects with and without rheumatoid arthritis. Methods: The ankle-brachial index (ABI) was measured at the posterior tibial and dorsal pedal arteries. Arteries were classified as obstructed with ABI (0.9, normal with ABI .0.9 but (1.3, and incompressible with ABI .1.3. Multinomial logistic regression was used to estimate differences in ABI between patients and controls, adjusting for cardiovascular risk factors, rheumatoid arthritis manifestations, inflammation markers, and glucocorticoid dose. Results: 234 patients with rheumatoid arthritis and 102 controls were studied. Among the rheumatoid patients, 66 of 931 arteries (7%) were incompressible and 30 (3%) were obstructed. Among the controls, three of 408 arteries (0.7%) were incompressible (p = 0.002) and four (1%) were obstructed (p = 0.06). At the person level, one or more abnormal arteries occurred among 45 rheumatoid patients (19%), v five controls (5%, p = 0.001). The greater frequency of arterial incompressibility and obstruction in rheumatoid arthritis was independent of age, sex, and cardiovascular risk factors. Adjustment for inflammation markers, joint damage, rheumatoid factor, and glucocorticoid use reduced rheumatoid arthritis v control differences. Most arterial impairments occurred in rheumatoid patients with 20 or more deformed joints. This subgroup had more incompressible (15%, p(0.001) and obstructed arteries (6%, p = 0.005) than the controls, independent of covariates. Conclusions: Peripheral arterial incompressibility and obstruction are increased in rheumatoid arthritis. Their propensity for patients with advanced joint damage suggests shared pathogenic mechanisms.